Consequences Associated With Obstructive Sleep Apnea (OSA)

The present results showed that daily protection with caffeine attenuated the increase in MDA levels in AlCl3-intoxicated rats. Supporting the present finding, previous studies have revealed the antioxidant potential of caffeine against lipid peroxidation in various animal models of neurologic diseases, including Alzheimer’s disease (Prasanthi et al., 2010), epilepsy (Souza et al., 2013) and Parkinson's disease (Khadrawy et al., 2017). It has been demonstrated that caffeine has the ability to scavenge reactive oxygen species (Devasagayam et al., 1996) and modulated the brain antioxidant system through increasing the content of GSH and activities of antioxidant enzymes like glutathione reductase and superoxide dismutase (Abreu et al., 2011). Generally, the antioxidant capacity of caffeine was similar to that of the established biological antioxidant GSH and significantly higher than ascorbic acid (Devasagayam et al., 1996). Accordingly, this may explain the ability of caffeine to attenuate lipid peroxidation induced by AlCl3 in the current study via direct scavenging of reactive oxygen species or by increasing GSH content and antioxidant enzymes activities.

of sleep apnea are obstructive sleep apnea (OSA), central sleep apnea (CSA), and complex sleep

distant ancestors out of harms way during the night when they could not see as

Excess weight. More than half of those with obstructive sleep apnea are overweight. Fat deposits around your upper airway may obstruct your breathing. However, not everyone who has sleep apnea is overweight and vice versa. Thin people can develop the disorder, too.

Each of these partially reduced, or reactive nitrogen species (RNS), possesses its own particular reactivity.NO and its isoforms are capable of reacting with a number of biological molecules, however, for the purpose of this review we will restrict our discussion to those that have been implicated in cellular signaling within the nervous system. NO reaction with proteins can be divided into three broad and basic pathways, namely reaction with (1) metals, (2) oxides, and (3) thiols. In the following section we will consider the reactivity involved in each of these

Nitric oxide synthase have been implicated in many aspects of human development and disease. Inhibition of iNOS or lowered levels of NO have been shown to help prevent ischaemic brain injury (4), reduce cellular markers of inflammation in osteoarthritis (5), speed differentiation and decrease survival of embryonic stem cells (6), reduction in IBS inflammation (7), protection from Alzheimer’s like symptoms in mice (8), and changes in cardiovascular function

The results presented here are logical extension of previous studies focusing on Nrf2 as a control point for the maintenance of GSH homeostasis in response to E-induced redox shifts in cultured neurons and in the developing brain. The Nrf2-related studies illustrated that the transcription factor does play a vital role in neuroprotection against E damage [7]. Yet, the neuroprotective setting remained incomplete in that GSH homeostasis was not preserved in a subpopulation of neurons in the E-exposed fetal brain [7], even in the presence of E-dependent up-regulation of Nrf2 expression. To mitigate this gap in our understanding, these new studies address a role of Cys homeostasis and their control points which could be

The hypoxia-inducible factor prolyl hydroxylase domain enzymes (HIF-PHDs) are a family of oxygen sensors that has been implicated in neuronal survival. Catalysis by the HIF-PHDs destabilizes the transcriptional activator HIF-1a under normoxia. HIF-PHDs are promising target candidates for mitochondrial protection in paradigms of oxidative stress. The inhibition of HIF-PHDs prevented neuronal cell death induced by mitochondrial toxins [1][2].

Obstructive sleep apnea: it’s a serious condition in which the upper airways get obstructed during sleep. The upper airways can be blocked by excess tissue such as, large tonsils or large tongue. Furthermore, the airway muscles can contribute to the condition by relaxing and collapsing during sleep. The interruption of breathing can initiates impulses from the brain to wake to person to restart the breathing process.[3]

The blood-brain barrier (BBB) is a metabolic and physical barrier between the central nervous system and the brain blood flow (1). The correct functioning of the BBB is crucial for keeping brain homeostasis and avoiding many poisons and pathogens (2). During cerebral ischemia, BBB disruption is a crucial event that induces an influx of water, resulting in vasogenic edema (3), and causes supplementary brain harm such as dementia through accumulation of beta-amyloid peptide (4). Brain edema aggravates the development of infarct development and causes herniation and loss of life (5). It's been reported that reactive oxygen species (ROS) exert deleterious activities, such as BBB disruption and BBB hyperpermeability, during vasogenic edema (6).

Before 1980s, Nitric oxide (NO) was only known as a colorless and toxic gas. Because NO vigorously reacts with atmospheric ozone and depletes the protection of ozone layer. Moreover, it reacts with atmospheric water and creates acidic precipitations. NO was considered to be environmentally hazardous until 1987 when it was discovered to be generated by human body. And it was in 1992 that NO was voted the molecule of the year and extensive research has been centering on the role of NO biological events. NO even brought Louis J. Ignerro, Robert F. Furchgott and Ferid Murad the Nobel Prize for Medicine and Physiology in 1998 for the identification of NO as a signaling molecular in the cardiology[1].

A/the central regulator of GSH homeostasis, hence redox balance mitigation of neuron apoptotic death [5], is the master transcription factor, nuclear factor E2-related factor 2 (Nrf2). Nrf2 regulated genes include glutamate-cysteine ligase (GCL) (rate limiting enzyme in GSH synthesis), glutathione reductase (generation of reduced/active GSH), and multiple components of the gamma glutamyl cycle by which the GSH synthesis substrate, Cys is supplied to neurons in addition to dietary source(s) [20, 25]. Previous study in our laboratory addressed Nrf2/ARE (Antioxidant Response Element)-mediated neuroprotection which should prevent neuron death by maintaining GSH homeostasis [7]. E does up-regulate Nrf2 and the knockout of Nrf2 illustrated that this increase in Nrf2 confers a certain degree of neuroprotection [7]. However, somehow E prevents Nrf2 from providing complete protection and a population of fetal neurons still succumbs unless we artificially increase Nrf2 beyond its innate capacity [7].

Nitric oxide (NO) is an important cellular signaling molecule that participates in diverse physiological functions in mammals, including vasodilation, smooth muscle relaxation, neurotransmission, and the immune response. NO, a free radical, is produced by a family of enzymes called nitric oxide synthases (NOS) by the oxidation of L-arginine to L-citrulline. There are three isoforms of NOS. Two of them, neuronal NOS (nNOS) and endothelial NOS (eNOS), are constitutively expressed, while the third one is inducible and is thus termed iNOS. nNOS is primarily found in the nervous system and is necessary for neuronal signaling, while eNOS is localized to the endothelium and is essential for vasodilation and control of blood pressure (5). These two isoforms produce nanomolar amounts of NO for short periods of time (seconds to minutes) in a calcium/calmodulin (CaM)-dependent manner (1, 91, 189).

The dental profession should have a role in the diagnosis and treatment of sleep apnea. Sleep apnea is divided into two categories being Obstructive sleep apnea and Central sleep apnea. Obstructive sleep apnea is a disorder in which the flow of air pauses or decreases multiple times during your sleep affecting the airway becoming narrowed, or blocked. A sudden pause in your breathing cycle is called an apnea episode. A decrease in the airflow while breathing as your asleep is called a hypopnea episode. Central sleep apnea is also a disorder in which your breathing patterns constantly stops and starts throughout a night. Central sleep apnea occurs most because your brain does not send the correct signals to the necessary muscles that help control

During ischemia, adenine nucleotide catabolism results in an increase the intracellular concentration of hypoxanthine, which is then converted into toxic reactive oxygen species (ROS) upon the reoxygenation of tissue(Collard et al.,2001).